Apte Minoti V, Pirola Romano C, Wilson Jeremy S
Pancreatic Research Group, South-western Sydney Clinical School, Liverpool Hospital, Sydney, Australia.
J Gastroenterol Hepatol. 2006 Oct;21 Suppl 3:S97-S101. doi: 10.1111/j.1440-1746.2006.04587.x.
Pancreatic stellate cells (PSC) are now recognized as the key mediators of pancreatic fibrosis, a characteristic feature of chronic pancreatitis. The role of PSC in alcoholic pancreatic fibrosis has been examined in vivo (using pancreatic tissue from patients with alcohol-induced chronic pancreatitis and from animal models of experimental pancreatitis) and in vitro (using PSC in culture). These studies indicate that PSC are activated early in the course of pancreatic injury and are the predominant source of collagen in the fibrotic pancreas. The factors responsible for mediating PSC activation during chronic alcohol exposure include ethanol, its metabolite acetaldehyde, oxidant stress and cytokines (released during episodes of alcohol-induced pancreatic necroinflammation). Most recently, the intracellular signaling mechanisms regulating ethanol-induced PSC activation have been identified and include the mitogen-activated protein kinase (MAPK) pathway, phosphatidylinositol-3-kinase (PI3K) and protein kinase C (PKC), and the transcription factor activator protein-1 (AP-1).
胰腺星状细胞（PSC）现已被公认为胰腺纤维化的关键介质，胰腺纤维化是慢性胰腺炎的一个特征性表现。PSC在酒精性胰腺纤维化中的作用已在体内（使用酒精性慢性胰腺炎患者的胰腺组织以及实验性胰腺炎动物模型）和体外（使用培养的PSC）进行了研究。这些研究表明，PSC在胰腺损伤过程中早期被激活，并且是纤维化胰腺中胶原蛋白的主要来源。在慢性酒精暴露期间介导PSC激活的因素包括乙醇、其代谢产物乙醛、氧化应激和细胞因子（在酒精性胰腺坏死性炎症发作期间释放）。最近，已确定调节乙醇诱导的PSC激活的细胞内信号传导机制，包括丝裂原活化蛋白激酶（MAPK）途径、磷脂酰肌醇-3-激酶（PI3K）和蛋白激酶C（PKC），以及转录因子激活蛋白-1（AP-1）。
